2. Hemorrhoids
• Variceal dilations of the anal and perianal
venous plexuses form collaterals that connect
the portal and caval venous systems
• Affect about 5% of the general population
Causes:
– PHT
– Constipation (straining at stool)
– Venous stasis of pregnancy
3. Types
• External hemorrhoids: Dilatation of collateral
vessels within the inferior hemorrhoidal
plexus [located below the anorectal line]
• Internal hemorrhoids: those that result from
dilation of the superior hemorrhoidal plexus
within the distal rectum
6. Histology
• Thin-walled, dilated, submucosal vessels that
protrude beneath the anal or rectal mucosa
• They are subject to trauma:
– Inflammation
– Thrombosis
– Superficial ulceration
25. Morphology
• Congested serosal blood vessels
• Normal glistening serosal surface turns into a dull, granular
and erythematous
• Hall mark of Acute appendicitis:
• Diagnosis of acute appendicitis requires neutrophilic infiltration
of the muscularis propria
• Other features:
• Mucosal ulceration
• Luminal exudation
• Fibrinopurulent exudate on the serosa
• Acute suppurative appendicitis
• Acute gangrenous appendicitis
26.
27. Hall mark of Acute appendicitis:
Diagnosis of acute appendicitis requires neutrophilic
infiltration of the muscularis propria
28. Clinical Features
• Pain:
– Early acute appendicitis: Periumbilical
– Later: Localizes to the right lower quadrant
• Classic physical finding is McBurney's sign
• Complications of appendicitis:
– Perforation
– Pyelophlebitis
– Portal venous thrombosis
– Liver abscess and
– Bacteremia
29. Tumors of the Appendix
CarcinoidCarcinoid
• The most common tumor of the appendix is
the carcinoid
• Usually discovered incidentally
• Usually involves the distal tip of the appendix
• 2 to 3 cm in diameter
• Nodal metastases are infrequent, and distant
spread is rare
38. Inflammatory Disease
Peritonitis may result from bacterial invasion or
chemical irritation and is most often due to:
•Leakage of bile or pancreatic enzymes, which
produces sterile peritonitis
– Perforation or rupture of the biliary system
– Acute hemorrhagic pancreatitis
•Foreign material
•Endometriosis
•Ruptured dermoid cysts
•Perforation of abdominal viscera
39. TumorsTumors
Primary tumors:
•Mesotheliomas
– Asbestos exposure
•Desmoplastic small round cell tumor (DSCRT)
– t(11;22)(p13;q12)
Secondary tumors: quite common
•Ovarian adenocarcinoma
•Pancreatic adenocarcinoma
•Gastric carcinoma
•Appendiceal mucinous carcinomas
•Wide variety of tumors of extra-abdominal origin
An additional differentiation pattern, termed basaloid, is present in tumors populated by immature cells derived from the basal layer of transitional epithelium ( Fig. 17-54B ). When the entire tumor displays a basaloid pattern, the archaic term cloacogenic carcinoma is still often applied.
Basaloid (Cloacogenic) Carcinoma Mimicking Intraabdominal Abscess: Report of a Case and Review of the Literature
Bottom Line: We performed Hartman procedure since the mass was nonresectable.Histopathological examination showed CC.As a result, the patient was lost because of multiple organ dysfunction syndrome that developed 3 months after radio-chemotherapy.
Affiliation: Department of Surgery, Diyarbakır Education and Research Hospital, Diyarbakır, Turkey.
Abstract: Cloacogenic carcinoma (CC, basaloid carcinoma) generally occurs around the dentate line, rarely it can arise from the other sides of the colon. There are only 5 cases of CC located outside the anal canal in the literature. The first occurrence of a CC presents as intraabdominal abscess. We describe a 23-year-old male patient who was admitted with fever and severe abdominal pain. Computed tomography imaging showed diffuse wall thickening about 10-11 cm above the rectosigmoid junction, intraabdominal abscess and a soft tissue lession covering the pelvis with a size of 8 × 8.5 cm including cystic necrotic areas. We performed Hartman procedure since the mass was nonresectable. Histopathological examination showed CC. In total, three times radiotherapy and a concurrent three-drug regimen of irinotecan, fluorouracil and folinic acid chemotherapy were administered for 6 weeks. As a result, the patient was lost because of multiple organ dysfunction syndrome that developed 3 months after radio-chemotherapy.
Mentions: Laparatomy was performed. An 8 × 5 cm abscess was seen related to the fistula tract on the anterior wall of the abdomen. No intestinal content was observed in the abdomen. A 10 cm mass attached to nearby tissues that contained necrotic and caseated areas covered the distal sigmoid and proximal rectum. We analyzed frozen sections from the mass during the operation. Atypical cells were seen in the frozen sections. We performed abscess drainage because of these results. As resection was not possible, Hartman-type proximal end colostomy was performed and the operation was ended leaving a distal ‘stubby’. As adenoid structures in patches were observed by histopathological examination, the differential diagnosis was made between poorly differentiated adenocarcinoma and CC. Immunohistochemically, staining with high-molecular-weight cytokeratin (HMWCK) (fig. 3), p63 antibody (fig. 4) and hematoxylin-eosin (fig. 5) confirmed the diagnosis of CC. On examination, CEA and CA 19-9 levels were normal (1.1 ng/ml and 2 IU/ml, respectively). Three weeks after discharge from the hospital, a 5-fluorouracil + folinic acid + irinotecan regimen was started. In total, three cycles of radiotherapy and a concurrent three-drug chemotherapy regimen (FOLFIRI; folinic acid, fluorouracil, irinotecan) were administered to the patient over 6 weeks. In CT scans 3 months after therapy, an increase in mass size and hydroureteronephrosis were observed. At the end of the fifth month, the patient's general condition deteriorated and sepsis developed. Subsequently, the patient died due to multiple organ dysfunction syndrome.
Figure 1 The lesion originated as condylomata acuminata and evolved into a Buschke–Löwenstein tumour over a period of 10 years as the patient refused treatment.
mesenteric lymphadenitis (often secondary to unrecognized Yersinia infection or viral enterocolitis), acute salpingitis, ectopic pregnancy, mittelschmerz (pain caused by minor pelvic bleeding at the time of ovulation), and Meckel diverticulitis
Ischemic injury and stasis of luminal contents, which favor bacterial proliferation, trigger inflammatory responses including tissue edema and neutrophilic infiltration of the lumen, muscular wall, and periappendiceal soft tissues.
Mucocele from mucinous cystadenoma of the appendixAxial contrast-enhanced CT scan performed in a patient with fever and right lower quadrant pain, shows an oval cystic mass with parietal thickening, that is continuous with the cecum (red arrows). The adjacent mesenteric fat has an increased density, due to coexistent inflamation. Macroscopy is shown. The hystological analysis revealed a mucinous cystadenoma with coexistent mucocele and inflamation.
Peritonitis may result from bacterial invasion or chemical irritation and is most often due to:
• Leakage of bile or pancreatic enzymes, which produces sterile peritonitis
• Perforation or rupture of the biliary system that evokes a highly irritating peritonitis, usually complicated by bacterial superinfection
• Acute hemorrhagic pancreatitis (see Chapter 19 ), which is associated with leakage of pancreatic enzymes and fat necrosis. Globules of fat may be found in the peritoneal fluid. Damage to the bowel wall may allow bacteria to spread to the peritoneal cavity, leading to a frank suppurative exudate after 24 to 48 hours.
• Foreign material, including that introduced surgically (e.g., talc and sutures), that induces foreign body–type granulomas and fibrous scarring
• Endometriosis, which causes hemorrhage into the peritoneal cavity, where it acts as an irritant
• Ruptured dermoid cysts release keratins that invoke an intense granulomatous reaction
• Perforation of abdominal viscera.